These changes during PD have potentially important implications for stroke as systemic inflammation unequivocally worsens ischemic damage,46,47 and IL-1β has a well-documented central role in the acute phases post-stroke.43,47,61 IL-17A has also been implicated in perpetuating damage after stroke; trafficking of IL-17+ γδ T cells to the ischemic brain is associated with worse outcome.62, –64 In contrast, GM-CSF is reportedly neuroprotective after stroke,65 indicating a potentially complex role for the IL-17A:GM-CSF axis in ischemic brain damage. The gene discussed is CSF2; the disease is stroke disorder.